학술논문
Response to Comments on “Aberrant type 1 immunity drives susceptibility to mucosal fungal infections”
Document Type
article
Author
Break, Timothy J; Oikonomou, Vasileios; Dutzan, Nicolas; Desai, Jigar V; Swidergall, Marc; Freiwald, Tilo; Chauss, Daniel; Harrison, Oliver J; Alejo, Julie; Williams, Drake W; Pittaluga, Stefania; Lee, Chyi-Chia R; Bouladoux, Nicolas; Swamydas, Muthulekha; Hoffman, Kevin W; Greenwell-Wild, Teresa; Bruno, Vincent M; Rosen, Lindsey B; Lwin, Wint; Renteria, Andy; Pontejo, Sergio M; Shannon, John P; Myles, Ian A; Olbrich, Peter; Ferré, Elise MN; Schmitt, Monica; Martin, Daniel; Core16, Genomics and Computational Biology; Barber, Daniel L; Solis, Norma V; Notarangelo, Luigi D; Serreze, David V; Matsumoto, Mitsuru; Hickman, Heather D; Murphy, Philip M; Anderson, Mark S; Lim, Jean K; Holland, Steven M; Filler, Scott G; Afzali, Behdad; Belkaid, Yasmine; Moutsopoulos, Niki M; Lionakis, Michail S
Source
Science. 373(6561)
Subject
Language
Abstract
Puel and Casanova and Kisand et al. challenge our conclusions that interferonopathy and not IL-17/IL-22 autoantibodies promote candidiasis in autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy. We acknowledge that conclusive evidence for causation is difficult to obtain in complex human diseases. However, our studies clearly document interferonopathy driving mucosal candidiasis with intact IL-17/IL-22 responses in Aire-deficient mice, with strong corroborative evidence in patients.